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1 xpression of the full virulence potential of BHV-5.
2 with the gE5 epitope-reverted and wild-type BHV-5.
3 with the gE5 epitope-reverted and wild-type BHV-5.
4 similar to that of the Us9 rescue mutant of BHV-5.
5 differential neuropathogenesis of BHV-1 and BHV-5.
6 te genomic sequence of bovine herpesvirus 5 (BHV-5), an alphaherpesvirus responsible for fatal mening
7 ted BHV-1 and BHV-5 recombinants: gE-deleted BHV-5 (BHV-5gEDelta), BHV-5 expressing BHV-1 gE (BHV-5gE
8 nfected intranasally with gE epitope-deleted BHV-5 did not develop seizures, and only 20% of the infe
9 tranasal infection, the Us9 rescue mutant of BHV-5 displayed a wild-type level of neurovirulence and
10 combinants: gE-deleted BHV-5 (BHV-5gEDelta), BHV-5 expressing BHV-1 gE (BHV-5gE1), and BHV-1 expressi
15 tion, and immunohistochemistry indicate that BHV-5 gE is important for efficient neural spread and ne
17 predicted amino acid sequences of BHV-1 and BHV-5 gE open reading frames showed that they had 72% id
18 ificantly less efficiently in the brain than BHV-5 gE revertant or wild-type BHV-5, which produced se
23 a doublet of 17- and 19-kDa protein bands in BHV-5-infected cell lysates and in purified virions.
24 anterograde spread of bovine herpesvirus 5 (BHV-5) infection from the olfactory receptor neurons to
28 determine the role of the BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinan
30 V-1 and BHV-5, we have constructed BHV-1 and BHV-5 recombinants: gE-deleted BHV-5 (BHV-5gEDelta), BHV
32 erences, BHV-1 Us9 not only complemented for BHV-5 Us9 and rescued the anterograde-spread defect of t
33 BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinant was generated and its neu
39 ed, and the predicted amino acid sequence of BHV-5 Us9 was compared with the corresponding Us9 sequen
40 rescued the anterograde-spread defect of the BHV-5 Us9-deleted virus but conferred increased neurovir
42 tory pathway, but the Us9 deletion mutant of BHV-5 was virtually avirulent and failed to invade the C
43 e of the neurovirulent bovine herpesvirus 5 (BHV-5) was determined and compared with that of the nonn
44 differential neuropathogenesis of BHV-1 and BHV-5, we have constructed BHV-1 and BHV-5 recombinants:
45 e brain than BHV-5 gE revertant or wild-type BHV-5, which produced severe neurological signs in 70 to
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